Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (616 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A family of biologically active compounds derived from arachidonic acid by oxidative metabolism through the 5-lipoxygenase pathway. They participate in host defense reactions and pathophysiological conditions such as immediate hypersensitivity and inflammation. They have potent actions on many essential organs and systems, including the cardiovascular, pulmonary, and central nervous system as well as the gastrointestinal tract and the immune system.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Leukotriene.
Where it fits in the MeSH classification
- Broader topics
- Arachidonic Acids; Eicosanoids
- Narrower topics
- Leukotriene A4; Leukotriene B4; SRS-A
- See also
- Receptors, Leukotriene
Research landscape
PubMed indexes 14,753 records tagged with the MeSH heading “Leukotrienes” (counts retrieved 2026-10-31). 515 of them (3.5%) were published from 2020 onward, and the busiest period so far is through 1999 with 9,776 records.
Reviews account for 1,653 records (11.2%) and meta-analyses for 5. Randomized controlled trials number 363 (2.5%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 9,776 |
| 2000-2009 | 2,793 |
| 2010-2019 | 1,669 |
| 2020 onward | 515 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,653 | 11.2% |
| Meta-analyses | 5 | 0.0% |
| Randomized controlled trials | 363 | 2.5% |
Method: PubMed query "Leukotrienes"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Contributions of mast cells and vasoactive products, leukotrienes and chymase, to dengue virus-induced vascular leakage | 2013 | Research article Design not recorded in structured metadata | 144 | cc by PMID 23638300 · DOI · PMC3639510 |
| Alveolar Macrophages Prevent Lethal Influenza Pneumonia By Inhibiting Infection Of Type-1 Alveolar Epithelial Cells | 2017 | Research article Design not recorded in structured metadata | 116 | cc by PMID 28085958 · DOI · PMC5268648 |
| The Role of Leukotrienes as Potential Therapeutic Targets in Allergic Disorders | 2019 | Review article Design not recorded in structured metadata | 112 | cc by PMID 31336653 · DOI · PMC6679143 |
| Intestinal mast cell-derived leukotrienes mediate the anaphylactic response to ingested antigens | 2025 | Research article Design not recorded in structured metadata | 29 | cc by PMID 40773543 · DOI · PMC12513082 |
Contributions of mast cells and vasoactive products, leukotrienes and chymase, to dengue virus-induced vascular leakage [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Dengue Virus (DENV), a flavivirus spread by mosquito vectors, can cause vascular leakage and hemorrhaging.
- Closing excerpt
- 001.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (150 words)
Dengue Virus (DENV), a flavivirus spread by mosquito vectors, can cause vascular leakage and hemorrhaging. However, the processes that underlie increased vascular permeability and pathological plasma leakage during viral hemorrhagic fevers are largely unknown. Mast cells (MCs) are activated in vivo during DENV infection, and we show that this elevates systemic levels of their vasoactive products, including chymase, and promotes vascular leakage. Treatment of infected animals with MC-stabilizing drugs or a leukotriene receptor antagonist restores vascular integrity during experimental DENV infection. Validation of these findings using human clinical samples revealed a direct correlation between MC activation and DENV disease severity. In humans, the MC-specific product, chymase, is a predictive biomarker distinguishing dengue fever (DF) and dengue hemorrhagic fever (DHF). Additionally, our findings reveal MCs as potential therapeutic targets to prevent DENV-induced vasculopathy, suggesting MC-stabilizing drugs should be evaluated for their effectiveness in improving disease outcomes during viral hemorrhagic fevers. DOI:http://dx.doi.org/10.7554/eLife.00481.001.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 23638300 · DOI · PMC3639510
Alveolar Macrophages Prevent Lethal Influenza Pneumonia By Inhibiting Infection Of Type-1 Alveolar Epithelial Cells [2]
Abstract reading summary — source excerpts
- Opening excerpt
- The Influenza A virus (IAV) is a major human pathogen that produces significant morbidity and mortality.
- Closing excerpt
- The findings further suggest that the cysLT pathway and the receptors for cysLT metabolites represent potential therapeutic targets in severe IAV infection.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (244 words)
The Influenza A virus (IAV) is a major human pathogen that produces significant morbidity and mortality. To explore the contribution of alveolar macrophages (AlvMΦs) in regulating the severity of IAV infection we employed a murine model in which the Core Binding Factor Beta gene is conditionally disrupted in myeloid cells. These mice exhibit a selective deficiency in AlvMΦs. Following IAV infection these AlvMΦ deficient mice developed severe diffuse alveolar damage, lethal respiratory compromise, and consequent lethality. Lethal injury in these mice resulted from increased infection of their Type-1 Alveolar Epithelial Cells (T1AECs) and the subsequent elimination of the infected T1AECs by the adaptive immune T cell response. Further analysis indicated AlvMΦ-mediated suppression of the cysteinyl leukotriene (cysLT) pathway genes in T1AECs in vivo and in vitro. Inhibition of the cysLT pathway enzymes in a T1AECs cell line reduced the susceptibility of T1AECs to IAV infection, suggesting that AlvMΦ-mediated suppression of this pathway contributes to the resistance of T1AECs to IAV infection. Furthermore, inhibition of the cysLT pathway enzymes, as well as blockade of the cysteinyl leukotriene receptors in the AlvMΦ deficient mice reduced the susceptibility of their T1AECs to IAV infection and protected these mice from lethal infection. These results suggest that AlvMΦs may utilize a previously unappreciated mechanism to protect T1AECs against IAV infection, and thereby reduce the severity of infection. The findings further suggest that the cysLT pathway and the receptors for cysLT metabolites represent potential therapeutic targets in severe IAV infection.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28085958 · DOI · PMC5268648
The Role of Leukotrienes as Potential Therapeutic Targets in Allergic Disorders [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Leukotrienes (LTs) are lipid mediators that play pivotal roles in acute and chronic inflammation and allergic diseases.
- Closing excerpt
- This review summarizes the biology of LTs and their receptors, recent developments in the area of anti-LT strategies (in settings such as ongoing clinical studies), and prospects for future therapeutic applications.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (91 words)
Leukotrienes (LTs) are lipid mediators that play pivotal roles in acute and chronic inflammation and allergic diseases. They exert their biological effects by binding to specific G-protein-coupled receptors. Each LT receptor subtype exhibits unique functions and expression patterns. LTs play roles in various allergic diseases, including asthma (neutrophilic asthma and aspirin-sensitive asthma), allergic rhinitis, atopic dermatitis, allergic conjunctivitis, and anaphylaxis. This review summarizes the biology of LTs and their receptors, recent developments in the area of anti-LT strategies (in settings such as ongoing clinical studies), and prospects for future therapeutic applications.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31336653 · DOI · PMC6679143
Intestinal mast cell-derived leukotrienes mediate the anaphylactic response to ingested antigens [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Anaphylaxis is a life-threatening complication of food allergen exposure.
- Closing excerpt
- Mice genetically deficient in cysteinyl leukotriene synthesis, or those treated with the arachidonate 5-lipoxygenase (aLOX5) antagonist zileuton, were protected from oral antigen-induced responses, whereas those elicited by intravenous injection were unaltered.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (131 words)
Anaphylaxis is a life-threatening complication of food allergen exposure. Although mechanisms governing anaphylaxis after intravenous injection are defined in mice, these models neglect mucosal exposure that accompanies ingestion. We investigated the role of mast cells within the intestine of mice and found that oral anaphylaxis required immunoglobulin E-Fcε receptor 1 (IgE-FcεR1) signaling. Intestinal mast cells were a heterogeneous population, shaped by epithelial cues. Compared with connective tissue mast cells found throughout the body, intestinal mast cells largely resided in the epithelium, displayed divergent transcriptomes and effector functions, and had a diminished ability to generate histamine, but they enhanced leukotriene synthesis. Mice genetically deficient in cysteinyl leukotriene synthesis, or those treated with the arachidonate 5-lipoxygenase (aLOX5) antagonist zileuton, were protected from oral antigen-induced responses, whereas those elicited by intravenous injection were unaltered.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40773543 · DOI · PMC12513082
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Prostaglandins and leukotrienes: advances in eicosanoid biology [5]
- Research article Leukotrienes [6]
- Research article Lipoxygenase and leukotriene pathways: biochemistry, biology, and roles in disease [7]
- Research article Omega-6 fatty acids and inflammation [8]
- Research article The role of leukotrienes in inflammation [9]
- Research article 5-Lipoxygenase, a key enzyme for leukotriene biosynthesis in health and disease [10]
References
- St John AL, Rathore AP, Raghavan B, Ng ML, Abraham SN. Contributions of mast cells and vasoactive products, leukotrienes and chymase, to dengue virus-induced vascular leakage. . 2013. PMID 23638300 · DOI · PMC3639510
- Cardani A, Boulton A, Kim TS, Braciale TJ. Alveolar Macrophages Prevent Lethal Influenza Pneumonia By Inhibiting Infection Of Type-1 Alveolar Epithelial Cells. . 2017. PMID 28085958 · DOI · PMC5268648
- Jo-Watanabe A, Okuno T, Yokomizo T. The Role of Leukotrienes as Potential Therapeutic Targets in Allergic Disorders. . 2019. PMID 31336653 · DOI · PMC6679143
- Bachtel ND, Cullen JL, Liu M, Erickson SA, Kutyavin VI, El-Naccache DW, et al.. Intestinal mast cell-derived leukotrienes mediate the anaphylactic response to ingested antigens. . 2025. PMID 40773543 · DOI · PMC12513082
- Funk CD. Prostaglandins and leukotrienes: advances in eicosanoid biology. Science. 2001. PMID 11729303 · DOI
- Peters-Golden M, Henderson WR. Leukotrienes. N Engl J Med. 2007. PMID 17978293 · DOI
- Haeggström JZ, Funk CD. Lipoxygenase and leukotriene pathways: biochemistry, biology, and roles in disease. Chem Rev. 2011. PMID 21936577 · DOI
- Innes JK, Calder PC. Omega-6 fatty acids and inflammation. Prostaglandins Leukot Essent Fatty Acids. 2018. PMID 29610056 · DOI
- Henderson WR. The role of leukotrienes in inflammation. Ann Intern Med. 1994. PMID 7944079 · DOI
- Rådmark O, Werz O, Steinhilber D, Samuelsson B. 5-Lipoxygenase, a key enzyme for leukotriene biosynthesis in health and disease. Biochim Biophys Acta. 2015. PMID 25152163 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.